• Ko-Hsiu Lu, Ko-Huang Lue, Hsien-Hua Liao, Keh-Liang Lin, and Jing-Gung Chung.
• Department of Orthopaedic Surgery, Chung Shan Medical University Hospital, 110, Section 1, Chien-Kuo N. Road, Taichung 402, Taiwan, Republic of China.
• Clin. Chim. Acta. 2005 Jul 1; 357 (1): 65-73.

BackgroundPaclitaxel, an antineoplastic drug, inhibits cell growth and cell cycle progression and induces apoptosis in human leukemia HL-60 cells. Caspase-3 plays a direct role in proteolytic cleavage of cellular proteins responsible for progression to apoptosis.MethodsWe examined the cell morphology and apoptosis in HL-60 cells after exposure to paclitaxel and measured caspase-3 activities with or without z-VAD-fmk (a broad-spectrum caspase inhibitor) pretreatment by flow cytometric analysis and Western blotting.ResultsTogether, our results were (1) paclitaxel mainly induced G2/M cell cycle arrest in HL-60 cells (p<0.001); (2) time (p<0.001)- and dose-dependent (p<0.001) apoptosis of HL-60 cells was induced by paclitaxel; (3) in HL-60 cells, z-VAD-fmk blocked paclitaxel-induced apoptosis (12 h: p<0.001; 24 h: p<0.01; 48 h: p<0.01; 72 h: p<0.001) and caspase-3 activation (12 h: p<0.05; 24 h: p<0.01; 48 h: p<0.01; 72 h: p<0.01).ConclusionsThese results suggest that paclitaxel can induce G2/M cell cycle transition and apoptosis via caspase-3 activity in HL-60 cells.

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